Faculty mentor/PI email address
pittonrissardo-jamir@cooperhealth.edu
Keywords
Manganese, manganism, serum, cerebrospinal fluid, Parkinson's disease, parkinsonism
Date of Presentation
5-6-2026 12:00 AM
Poster Abstract
Background: Manganese (Mn) exposure can cause parkinsonism, but circulating and cerebrospinal fluid (CSF) Mn levels in idiopathic Parkinson’s disease (PD) have been reported inconsistently. This study aims to determine whether Mn concentrations differ between patients with PD. Methods: A systematic review of PubMed/Medline studies reporting CSF/serum Mn concentrations in PD was done. Random‑effects models with inverse‑variance weighting were used to pool mean differences (MDs). Studies were stratified a priori by analytical method. Results: For CSF Mn, the overall pooled effect showed no significant difference between PD and controls (MD 0.08 μg/L, 95% CI −0.31 to 0.47; I2=85.7%). Subgroup analysis revealed that legacy AAS (MD 4.9 μg/L) studies reported higher Mn in PD, whereas modern ICP‑MS studies showed no difference. For serum Mn, pooling across all studies showed no significant difference (MD = 0.36 μg/L; 95% CI −1.54 to 2.26; I2= 95%). In a sensitivity analysis excluding the legacy study by Kanabrocki et al., the pooled effect was attenuated to near zero and remained non‑significant (MD −0.01 μg/L, 95% CI −0.10 to 0.09; I2=91.5%). Subgroup analyses indicated a nominal increase in PD only in legacy AAS studies (MD 5.05 μg/L, 95% CI 0.05 to 10.05; I2=92%), while early ICP (MD −0.18 μg/L, 95% CI −0.40 to 0.04; I2=58%) and modern ICP‑MS (MD = −0.01 μg/L; 95% CI −0.40 to 0.04) studies demonstrated no significant serum Mn difference. Conclusions: Across both CSF and serum, method‑robust contemporary ICP‑MS data show no measurable Mn imbalance in PD. Apparent elevations reported in older studies are likely driven by analytical artifacts rather than disease biology.
Disciplines
Medicine and Health Sciences | Nervous System Diseases
Included in
Cerebrospinal Fluid and Serum Manganese Levels in Parkinson’s Disease: A Method‑Stratified Meta‑analysis
Background: Manganese (Mn) exposure can cause parkinsonism, but circulating and cerebrospinal fluid (CSF) Mn levels in idiopathic Parkinson’s disease (PD) have been reported inconsistently. This study aims to determine whether Mn concentrations differ between patients with PD. Methods: A systematic review of PubMed/Medline studies reporting CSF/serum Mn concentrations in PD was done. Random‑effects models with inverse‑variance weighting were used to pool mean differences (MDs). Studies were stratified a priori by analytical method. Results: For CSF Mn, the overall pooled effect showed no significant difference between PD and controls (MD 0.08 μg/L, 95% CI −0.31 to 0.47; I2=85.7%). Subgroup analysis revealed that legacy AAS (MD 4.9 μg/L) studies reported higher Mn in PD, whereas modern ICP‑MS studies showed no difference. For serum Mn, pooling across all studies showed no significant difference (MD = 0.36 μg/L; 95% CI −1.54 to 2.26; I2= 95%). In a sensitivity analysis excluding the legacy study by Kanabrocki et al., the pooled effect was attenuated to near zero and remained non‑significant (MD −0.01 μg/L, 95% CI −0.10 to 0.09; I2=91.5%). Subgroup analyses indicated a nominal increase in PD only in legacy AAS studies (MD 5.05 μg/L, 95% CI 0.05 to 10.05; I2=92%), while early ICP (MD −0.18 μg/L, 95% CI −0.40 to 0.04; I2=58%) and modern ICP‑MS (MD = −0.01 μg/L; 95% CI −0.40 to 0.04) studies demonstrated no significant serum Mn difference. Conclusions: Across both CSF and serum, method‑robust contemporary ICP‑MS data show no measurable Mn imbalance in PD. Apparent elevations reported in older studies are likely driven by analytical artifacts rather than disease biology.